Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray and ChIP-chip of Rrm3-Flag in wild-type and npl3 cells, and ChIP-chip of Npl3-Myc in wild type cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Saccharomyces cerevisiae Schizosaccharomyces pombe

PROVIDER: GSE50187 | GEO | 2013/11/15

SECONDARY ACCESSION(S): PRJNA217035

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microarray and ChIP-chip of Rrm3-Flag in wild-type and npl3 cells, and ChIP-chip of Npl3-Myc in wild type cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-11-15 | E-GEOD-50187 | biostudies-arrayexpress

ChIP-chip data of Npl3-Myc and Rrm3-Flag in wild-type and npl3∆ cells

2013-11-15 | GSE50185 | GEO

ChIP-chip data of Npl3-Myc and Rrm3-Flag in wild-type and npl3M-bM-^HM-^F cells

Project description:Transcription is a major obstacle for replication fork progression and a cause of genome instability. Such instability increases in mutants with a suboptimal assembly of the nascent messenger ribonucleo-protein particle (mRNP), as THO/TREX and some heterogeneous nuclear ribonucleoproteins (hnRNPs) mutants. Here we show that yeast npl3M-bM-^HM-^F cells show genome-wide replication obstacles as determined by accumulation of the Rrm3 helicase. Such obstacles preferentially occur at long and highly expressed genes, to which Npl3 is preferentially bound in wild-type cells. ChIP-chip studies were perfomed with antibodies against Myc-tagged Npl3 protein in wild-type cells of the yeast S. Cerevisiae, as well as Flag-tagged Rrm3 protein in both wild-type and npl3M-bM-^HM-^F cells.

2013-11-15 | E-GEOD-50185 | biostudies-arrayexpress

ChIP-chip data of Rrm3-Flag in wild-type and rpb1-1 cells

Project description:Transcription is a major contributor to genome instability.A main cause of transcription-associated instability relies on the capacity of transcription to stall replication. Such genome instability is increased in RNAPII mutants. ChIP-chips performed in asynchronous cultures showed an increase of the Rrm3 binding signal all over the genome in rpb1-1 compared to wild-type.

2014-12-04 | GSE55184 | GEO

ChIP-chip data of Thp1-Flag and Sac3-Flag in wild-type cells, and Rrm3-Flag in sac3∆ and thp1∆ cells

2014-10-08 | GSE56700 | GEO

ChIP-chip data of Rrm3-Flag in wild-type and rpb1-1 cells

2014-12-04 | E-GEOD-55184 | biostudies-arrayexpress

ChIP-chip data of HA-Yra1 and Rrm3-Flag in wild-type and cells overexpressing YRA1

Project description:Transcription is a major obstacle for replication fork progression and a cause of genome instability. Yra1 is an essential nuclear factor of the evolutionarily conserved family of hnRNP-like export factors that when overexpressed impairs mRNA export and cell growth. Through this ChIP-chip analysis it is shown that Yra1 binds to active chromatin and is enriched at telomeres when it is overexpressed, in agreement with a possible role of this mRNP factor in the maintenance of telomere integrity. Our data indicate that YRA1 overexpression correlates with replication impairment as inferred by the increase of Rrm3, a helicase involved in the replication fork progression, at transcribed genes and telomeres.

2016-03-11 | GSE68486 | GEO

ChIP-chip data of HA-Yra1 and Rrm3-Flag in wild-type and cells overexpressing YRA1

2016-03-11 | E-GEOD-68486 | biostudies-arrayexpress

ChIP-chip data of Thp1-Flag and Sac3-Flag in wild-type cells, and Rrm3-Flag in sac3M-bM-^HM-^F and thp1M-bM-^HM-^F cells

Project description:Transcription is a major obstacle for replication fork progression and a cause of genome instability. Such instability increases in mutants with a suboptimal assembly of the nascent messenger ribonucleo-protein particle (mRNP), as THO/TREX and the NPC-associated THSC/TREX-2 complex. Here we show that yeast sac3M-bM-^HM-^F and thp1M-bM-^HM-^F cells accumulate genome-wide replication obstacles as determined by the distribution of the Rrm3 helicase. Such obstacles preferentially occur at long and highly expressed genes, to which Sac3 and its interacting partner Thp1 are preferentially bound in wild-type cells. ChIP-chip studies were perfomed with antibodies against Flag-tagged Thp1 and Sac3 proteins in wild-type cells of the yeast S. Cerevisiae, as well as Flag-tagged Rrm3 protein in sac3M-bM-^HM-^F and thp1M-bM-^HM-^F cells that were compared with Rrm3 in wild-type cells from Santos-Pereira et al., 2013 (accession number GSE50185).

2014-10-08 | E-GEOD-56700 | biostudies-arrayexpress

Enhanced CLIP-Seq (eCLIP-Seq) of FLAG-tagged wild-type and mutant MYC in U2OS-MYC-KO-MYC-Tet-On cells

Project description:Transcription factor (TF) MYC binds to thousands of gene regulatory elements in the genome such as promoters and enhancers and exerts an amplification effect on the expression of most genes, regardless of the E-box motif existence. In this study, we discovered that MYC is an RNA-binding protein with a high affinity to guanosine-rich RNAs. RNAs that bind to MYC increase MYC’s chromatin occupancy, which helps with MYC-mediated regulation of gene expression. Mechanistically, two highly conserved sequences, amino acids 355-357 and 364-367, in the basic region of MYC are essential for RNA binding. Notably, alanine substitution of Lys355, Arg356, and Arg357 of MYC abolishes its RNA binding function but does not influence its complex formation ability, and E-box binding capacity of MYC:MAX dimer in vitro. However, loss of RNA binding function alone decreases MYC recruitment at gene regulatory elements in vivo, followed by a decreased MYC:MAX chromatin binding at these regions. This process further attenuates MYC-mediated gene expression. Therefore, RNA-binding-deficient MYC is compromised in promoting cancer cell proliferation. By demonstrating the mechanism of MYC-RNA interaction and the fundamental role of RNA binding activity in MYC-centric functions, our study reveals a new paradigm to MYC function and highlights an essential and probably general role of RNA binding capacity of TFs for their gene regulatory function.

2025-05-08 | GSE273775 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data